renal artery stenosis

Question 1

def of renal artery stenosis

Answer 1

stenosis of the renal artery - narrowing of the renal artery lumen - angiographically significant of >50% reduction in vessel diameter

Ischaemic nephropathy is a chronic reduction in glomerular filtration rate that occurs from a narrowing in the renal artery.

Question 2

aetiology of renal artery stenosis

Answer 2

atherosclerosis - older pt

• widespread aortic disease involving renal artery ostia
• dm
• dyslipidaemia
• smoking

fibromuscular dysplasia - younger pt

• of unknown aetiology may be associated with collagen disorders, neurofibromatosis and Takayasu’s disease
• may be associated with micro-aneurysms in the mid and distal renal arteries - resembling string of beads on angiography
• medial fibroplasia - histological finding in 90% cases
• intimal and adventitial fibroplasia - less common
• smoking

Question 3

pathophysiology of renal artery stenosis

Answer 3

activation of RAAS = increased systemic vascular resistance and Na retention

when stenosis leaves <50% reduction in vessel diameter - RAAS fail = worse kidney func and difficult to control HTN

Underperfusion of the kidney caused by blood flow obstruction produces adaptive changes in the kidney, including atrophy of tubular cells, fibrosis of the capillary tuft, and intra-renal arterial medial thickening

Angiotensin II stimulates fibroblast activity, = fibrosis in the glomerular tuft and in the tubules.

activation of the sympathetic nervous system, abnormalities in endothelial nitric oxide, endothelin release, and increased oxidative stress

Hypertension can cause hyalinosis, mesangial cell expansion, and growth factor release = fibrosis

Bilateral RAS results in volume overload with inappropriately elevated levels of renin.

atherosclerotic RAS

• involves the ostial and proximal 3rd of the renal artery
• endothelial injury and atherogenesis
• spontaneous or iatrogenic atheroemboli may further deteriroate kidney func

fibromuscular dysplasia

• May be focal, occurring in any part of the artery, or multifocal (alternating areas of stenosis and dilation [the so-called ‘string of beads’], which usually occurs in the mid and distal portions of the artery).

Question 4

pathology of RAS

Answer 4

Renal hypoperfusion stimulates the renin-angiotensin system leading to increasing circulating angiotensin II and aldosterone

= high BP

= fibrosis, glomerulosclerosis and renal failure

Question 5

epidemiology of RAS

Answer 5

Prevalence is unknown but believed to account for 1–5% of all hyper-tension;

fibromuscular dysplasia occurs mainly in women with hypertension at<45 years.

Fibromuscular dysplasia accounts for 10% of clinical RAS

Atherosclerotic RAS accounts for 90% of all RAS, Prevalence is as high as 25% in patients with CAD undergoing cardiac catheterisation.

Question 6

sx of RAS

Answer 6

history of HTN in <50yrs

HTN refractory to treatment

accelarated HTN and renal deterioration on starting ACEi

malignant htn

history of unexplained kidney dysfunction

history of multi-vessel coronary artery disease

history of PVD

history of flash pul oedema

Renovascular hypertension is hypertension mediated by high levels of renin and angiotensin II, produced by an underperfused kidney supplied by a stenosed renal artery.

Question 7

signs of RAS

Answer 7

HTN

signs of renal failure in advanced bilateral disease

an abnormal bruit over stenosed artery

Question 8

Ix for RAS

Answer 8

serum creatinine - normal or elevated

serum K - Hypokalaemia or low-normal potassium may suggest RAS due to activation of the renin-angiotensin system

urine analysis and sediment evaluation - normal in the absence of diabetic nephropathy or hypertensive glomerulosclerosis

aldosterone to renin ratio - Aldosterone-to-renin ratio <20 excludes primary aldosteronism as cause of hypertension and hypokalaemia or low-normal potassium. therefore find <20 in RAS

non-invasive

• Duplex ultrasound (technically difficult if obese).
• US measurement of kidney size (predicts outcome after revascularization, kidneys<8 cm are unlikely to improve).

CT angiography/MRI - risk of contrast nephrotoxicity

digital subtraction angiography - gold standard

renal scintigraphy

• Uses the radio-agent99Tc-DTPA (excreted by glomerular filtration) or99Tc -MAG3 (excreted by tubules
• Addition of an ACE inhibitor (captopril renography) causes delayed clearance by the affected kidney (may not be helpful if bilateral RAS).

Question 9

mx of atherosclerotic renal artery stenosis

Answer 9

1. modify atherosclerosis RFs
2. (ACE or ARB) target < 130/80
3. statin
4. aspirin
5. revascularisation - percurtaneous transluminal angioplasty with stenting - add clopidogrel after procedure / surgical revascularisation

Question 10

indications for percutaneous transluminal renal angioplasty

Answer 10

uncontrolled HTN despite meds
rapidly declining renal func
recurrent flash pul oedema
refractory HF

Question 11

indications for surgical revascularisation for RAS

Answer 11

complex or multiple lesions
concomitant aortic or renal aneurysms
failed percutaneous angioplasty

Question 12

mx of fibromuscular dysplasia -> RAS

Answer 12

1. ACEi
2. percurtaneous renal artery balloon angioplasty

consider stenting and dual antiplt therapy